Categories
Herbs & Plants

Polygonum bistorta

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Botanical Name :Polygonum bistorta or Persicaria bistorta
Family: Polygonaceae
Genus: Persicaria
Species: P. bistorta
Kingdom: Plantae
Order: Caryophyllales
Synonyms: Persicaria bistorta (L.) Samp., Polygonum ampliusculum Gand., Polygonum bistorta L., Polygonum bourdinii Gand., Polygonum carthusianorum Gand., Polygonum ellipticum Willd. ex Spreng., Polygonum pilatense Gand.

Common Name : Bistort or Common Bistort,  Meadow bistort, Snakeweed

Numerous other vernacular names have been recorded for the species in historical texts, though none is used to any extent. Many of the following refer to the plant’s use in making puddings: Adderwort, Dragonwort, Easter giant, Easter ledger, Easter ledges, Easter magiant, Easter man-giant, Gentle dock, Great bistort, Osterick, Oysterloit, Passion dock, Patience dock (this name is also used for Rumex patientia), Patient dock, Pink pokers, Pudding grass, Pudding dock, Red legs, Snakeweed, Twice-writhen, Water ledges.

Habitat :     Polygonum bistorta is native to northern and central Europe, including Britain, mountains of S. Europe, western and central Asia. It grows in damp meadows and by water, especially on acid soils.

Description:
Polygonum bistorta is a perennial plant, growing to 0.5 m (1ft 8in) by 0.5 m (1ft 8in) at a fast rate.   It  blooms  late spring into mid summer, producing tall stems ending in single terminal racemes that are club-like spikes of pink-rose colored flowers.  The seeds ripen from Aug to October. The flowers are hermaphrodite (have both male and female organs) and are pollinated by Insects.  The racemes are about 2 cm thick and 5-9 cm long and end 1 meter tall,upright growing stems. Plants grow in moist soils and under dry conditions go dormant, losing their foliage until adequate moisture exists again. This species is grown as an ornamental garden plant, especially the form ‘Superba’ which has larger, more showy flowers. Typically alpine plants growing from short, thick rhizomes that branch. The foliage is normally basal with a few smaller leaves produced near the lower end of the flowering stems. The leaves are oblong-ovate or triangular-ovate in shape and narrow at the base. The petioles are broadly winged.

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The Latin name “bistorta” refers to the twisted appearance of the root. In Northern England the plant was used to make a bitter pudding in Lent from a combination of the plant’s leaves, oatmeal, egg and other herbs. It is the principal ingredient of dock pudding or Easter-Ledge Pudding.  The root of Bistort can be used to produce an astringent that was used in medicine.

Cultivation:
Landscape Uses: Container, Ground cover. Succeeds in an ordinary garden soil[1] but prefers a moisture retentive not too fertile soil in sun or part shade. The plant repays generous treatment. A very cold-hardy plant, tolerating temperatures down to at least -25°c. Bistort was formerly cultivated as a medicinal and edible plant, though it has now fallen into virtual disuse. Plants are somewhat spreading, forming quite extensive colonies especially in low-lying pastures. They seem to be immune to the predations of rabbits. Special Features: Attractive foliage, Edible, Not North American native, Invasive, Suitable for cut flowers, Suitable for dried flowers.

Propagation:
Seed – sow spring in a cold frame. Germination is usually free and easy. When they are large enough to handle, prick the seedlings out into individual pots and plant them out in the summer if they have reached sufficient size. If not, overwinter them in a cold frame and plant them out the following spring after the last expected frosts. Division in spring or autumn. Very easy, larger divisions can be planted out direct into their permanent positions. We have found that it is better to pot up the smaller divisions and grow them on in light shade in a cold frame until they are well established before planting them out in late spring or early summer.

Edible Uses::…Edible Parts: Leaves; Root; Seed.
Leaves – raw or cooked. One report says that they are rather bitter[5], but we have found them to have a fairly mild flavour, especially when the leaves are young, though the texture is somewhat chewy when they are eaten raw. They make an excellent substitute for spinach. In Northern England the leaves are an ingredient of a bitter Lenten pudding, called Easter ledger pudding, that is eaten at Lent. The leaves are available from late winter in most years and can be eaten until the early autumn though they become much tougher as the season progresses. The leaves are a good source of vitamins A and C, a nutritional analysis is available. Seed – raw or cooked. The seed is very small and rather fiddly to utilize. Root – raw or cooked. Rich in starch and tannin, it is steeped in water and then roasted in order to reduce the tannin content. It is then said to be a tasty and nutritious food. The root has also been boiled or used in soups and stews and can be dried then ground into a powder and used in making bread. The root contains 30% starch, 1% calcium oxalate and 15 – 36% tannin.
Composition:
Figures in grams (g) or miligrams (mg) per 100g of food.
Leaves (Fresh weight)

*0 Calories per 100g
* Water : 82.6%
*Protein: 3g; Fat: 0.8g; Carbohydrate: 7.9g; Fibre: 3.2g; Ash: 2.4g;
*Minerals – Calcium: 0mg; Phosphorus: 0mg; Iron: 0mg; Magnesium: 0mg; Sodium: 0mg; Potassium: 0mg; Zinc: 0mg;
*Vitamins – A: 0mg; Thiamine (B1): 0mg; Riboflavin (B2): 0mg; Niacin: 0mg; B6: 0mg; C: 0mg;

Medicinal Uses:

Bistort is one of the most strongly astringent of all herbs and it is used to contract tissues and staunch blood flow. The root is powerfully astringent, demulcent, diuretic, febrifuge, laxative and strongly styptic. It is gathered in early spring when the leaves are just beginning to shoot, and then dried. It is much used, both internally and externally, in the treatment of internal and external bleeding, diarrhoea, dysentery, cholera etc. It is also taken internally in the treatment of a wide range of complaints including catarrh, cystitis, irritable bowel syndrome, peptic ulcers, ulcerative colitis and excessive menstruation. Externally, it makes a good wash for small burns and wounds, and is used to treat pharyngitis, stomatitis, vaginal discharge, anal fissure etc. A mouth wash or gargle is used to treat spongy gums, mouth ulcers and sore throats. The leaves are astringent and have a great reputation in the treatment of wounds. In Chinese medicine the rhizome is used for: epilepsy, fever, tetanus, carbuncles, snake and mosquito bites, scrofula and cramps in hands and feet . Considered useful in diabetes.

Roots and leaves were used to counteract poisons and to treat malaria and intermittent fevers. Dried and powdered it was applied to cuts and wounds to staunch bleeding, and a decoction in wine was taken for internal bleeding and diarrhea (especially in babies). It was also given to cause sweating and drive out the plague, smallpox, measles and other infectious diseases. Bistort is rich in tannins and one of the best astringents. Taken internally, it is excellent for bleeding, such as from nosebleeds, heavy periods and wounds, and for diarrhea and dysentery. Since it reduces inflammation and mucous secretions it makes a good remedy for colitis and for catarrhal congestion. It was originally recommended in 1917 as a treatment for debility with a tendency towards tuberculosis. It has also been used externally for pharyngitis, stomatitis, vaginal discharge, anal fissure, purulent wounds, hemorrhoids, mouth ulcers and gum disease. Comes well with Geranium maculatum.

Other Uses:......Tannin.……The roots contain up to 21% tannin

Known Hazards:   Although no specific mention has been made for this species, there have been reports that some members of this genus can cause photosensitivity in susceptible people. Many species also contain oxalic acid (the distinctive lemony flavour of sorrel) – whilst not toxic this substance can bind up other minerals making them unavailable to the body and leading to mineral deficiency. Having said that, a number of common foods such as sorrel and rhubarb contain oxalic acid and the leaves of most members of this genus are nutritious and beneficial to eat in moderate quantities. Cooking the leaves will reduce their content of oxalic acid. People with a tendency to rheumatism, arthritis, gout, kidney stones or hyperacidity should take especial caution if including this plant in their diet since it can aggravate their condition.

Disclaimer:
The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider.

Resources:
http://en.wikipedia.org/wiki/Persicaria_bistorta
http://www.herbnet.com/Herb%20Uses_AB.htm

http://www.pfaf.org/user/Plant.aspx?LatinName=Polygonum+bistorta

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Categories
Ailmemts & Remedies

Hypercalcaemia

Definition:-

Calcium is a mineral that’s vital for the development of healthy bones and teeth – 99 per cent of the calcium in our bodies is found here. It’s also needed for muscle contraction, regulation of the heartbeat and formation of blood clots. A long-term shortage of calcium can lead to osteoporosis (brittle-bone disease).

The four pea-sized parathyroid glands (found at the front of the neck) are responsible for regulating the body’s calcium levels. These small glands, which are embedded in the tissue of the thyroid gland in the neck, detect fluctuations in the level of calcium in the blood.

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There are times when this delicate balance is upset and too much calcium enters the blood. If levels rise too much, the glands decrease the secretion of the parathyroid hormone (PTH) and calcium levels return to normal again.
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Hypercalcaemia  is an elevated calcium level in the blood. (Normal range: 9–10.5 mg/dL or 2.2–2.6 mmol/L). It can be an asymptomatic laboratory finding, but because an elevated calcium level is often indicative of other diseases, a diagnosis should be undertaken if it persists. It can be due to excessive skeletal calcium release, increased intestinal calcium absorption, or decreased renal calcium excretion.

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Symptoms:
There is a general mnemonic for remembering the effects of hypercalcaemia: “groans (constipation), moans (psychic moans (e.g., fatigue, lethargy, depression)), bones (bone pain, especially if PTH is elevated), stones (kidney stones), and psychiatric overtones (including depression and confusion).”

Other symptoms can include fatigue, anorexia, nausea,abdominal pain, weightloss,loss of appetite, vomiting,constipation, pancreatitis and increased urination.

Abnormal heart rhythms can result, and ECG findings of a short QT interval and a widened T wave suggest hypercalcaemia. Significant hypercalcaemia can cause ECG changes mimicking an acute myocardial infarction.

Peptic ulcers may also occur.

Symptoms are more common at high calcium blood values (12.0 mg/dL or 3 mmol/l). Severe hypercalcaemia (above 15–16 mg/dL or 3.75–4 mmol/l) is considered a medical emergency: at these levels, coma and cardiac arrest can result.

Causes:-
One of the commonest causes of hypercalcaemia is cancer. Up to 20% of people with cancer have high calcium levels, especially with cancers of the breast, lung, head and neck, and certain blood cancers.

Abnormal parathyroid gland function:
*primary hyperparathyroidism
*solitary parathyroid adenoma
*primary parathyroid hyperplasia
*parathyroid carcinoma
*multiple endocrine neoplasia (MEN)
*familial isolated hyperparathyroidism
*lithium use
*familial hypocalciuric hypercalcaemia/familial benign hypercalcaemia

Malignancy:
*solid tumour with metastasis (e.g. breast cancer or classically squamous cell carcinoma, which can be PTHrP-mediated)
*solid tumour with humoral mediation of hypercalcaemia (e.g. lung cancer [in turn, most commonly of the small cell lung cancer type] or kidney cancer, pheochromocytoma)
*haematologic malignancy (multiple myeloma, lymphoma, leukaemia)

Vitamin-D metabolic disordershyper:
*vitaminosis D (vitamin D intoxication)
*elevated 1,25(OH)2D (see calcitriol under Vitamin D) levels (e.g. sarcoidosis and other granulomatous diseases)
*idiopathic hypercalcaemia of infancy
*rebound hypercalcaemia after rhabdomyolysis

Disorders related to high bone-turnover rateshyperthyroidism:
*prolonged immobilization
*thiazide use
*vitamin A intoxication
*Paget’s disease of the bone
*multiple myeloma

Renal failure
*severe secondary hyperparathyroidism:
*aluminium intoxication
*milk-alkali syndrome

Risk Factors:
An overproduction of PTH may also responsible for hypercalcaemia; this is often caused by a tumour in one or more of the parathyroid glands. Excess production of PTH may occur to compensate for a malfunction in one of the body’s other calcium-balancing mechanisms; for example, when the kidneys aren’t working properly or when there’s a deficiency of vitamin D.

Women over the age of 50 are most likely to have hypercalcemia, usually due to primary hyperparathyroidism.

Diagnosis:
Hypercalcaemia is diagnosed by laboratory tests including: serum calcium, albumin, phosphate, alkaline phosphate, BUN, creatinine, electrolytes and PTH level. These investigations assist in diagnosing the cause of hypercalcaemia and give a baseline indication of renal function. Urinary calcium should be measured as hypercalciuria may be detected. Other investigations may include an ECG and radiology examinations such as x-ray or bone scans which may show bone metastases

Treatment:
The treatment of hypercalcaemia is determined by the underlying disease, the degree of the hypercalcaemia and the patient’s clinical presentation. The aim of treatment is directed at decreasing serum calcium levels by increasing urinary excretion of calcium and decreasing bone resorption of calcium. Immobilization should be avoided as inactivity will cause an increase in bone resorption of calcium. The level of activity will be appropriate for the patient’s physical condition and other measures such as pain control may need to be considered prior to undertaking any physical activities. A review of the patient’s medications will need to be considered. Drugs that inhibit urinary calcium excretion, such as thiazide diuretics, should be ceased. NSAID and H2-receptor drugs, such as Ranitidine which decrease renal blood flow, should also be avoided if possible. Any calcium, Vitamin A and D supplements should also be ceased. Dietary restrictions of calcium have not been proven to be of any benefit to patients that are hypercalcaemic, or at risk of hypercalcaemia. Currently there is no data to suggest that hypercalcaemia has been attributed to food. However, some dietary supplements can cause abnormally hight levels of calcium in the blood. Patients with chronic renal failure are at risk of becoming hypercalacemic due to calcium intake.

This is due to decreased urine production, in combination with high calcium intake). Intravenous fluids (0.9% sodium chloride) will be administered to rehydrate the patient, the volume of fluid given will depend on the extent of the patients dehydration and cardiovascular and renal functions. At least 4-6 litres of saline on day 1, and 3-4 litres for several days thereafter is usual. Diuretics such as frusemide may also be given. Repeat blood tests should be taken several hours after treatment and reassessed. Cardiac status and urinary output should also be assessed, thus a strict fluid balance chart should be maintained on the patient. Oral phosphates, which inhibit bone resorption, may be administered. Diarrhoea is a common side effect and may lead to non-compliance. Bisphosphonates, which are given intravenously, inhibit osteoclast activity that contributes to bone resorption may also be administered. The two most common drugs used are Pamidronate/Aredia (60-90mg IV over 2 hours) and Zoledronic Acid/Zometa (4mg IV over 15 minutes). Both of these agents are generally well tolerated with limited side effects such as mild fever and irritation at the infusion site.

Prognosis:
The prognosis of hypercalcaemia depends upon the cause of increased calcium levels. When the underlying cause is treatable and the treatment is initiated promptly, hypercalcaemia can have a good prognosis. However, when associated with malignancy that has progressed into development of hypercalcemia, prognosis is poor. Hypercalcaemia is potentially fatal. Early diagnosis is important, as the cause of high blood calcium is usually identified and treated to avoid long-term complications. Signs and symptoms may be confused with those of end stage disease in terminal patients. In some patients, symptoms may be non-specific and have a slow onset.Some examples of these are:
•Anorexia
•Weakness
•Nausea
•Vomiting
•Constipation

In other cases, symptoms such as dehydration, renal failure and coma may develop very quickly resulting from very rapidly rising calcium levels. This may result in a life threatening situation. Symptoms do not always correlate with serum calcium levels. These must be closely compared with an in-depth patient history, examination and laboratory report. Signs and symptoms of hypercalcaemia can be numerous and nonspecific. They depend on the underlying cause and how quickly the calcium level rises. Mild hypercalcaemia may be asymptomatic but as the calcium levels rise, the symptoms begin to appear in all body systems. Some non-specific findings associated with hypercalcaemia include: decreased heart rate, hypertension, proximal muscle weakness (chronic hypercalcaemia), bony tenderness, increased tendon reflexes, unwanted tongue movements, dehydration and even coma.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Resources:
http://www.bbc.co.uk/health/physical_health/conditions/hypercalcaemia1.shtml
http://en.wikipedia.org/wiki/Hypercalcaemia
http://www.virtualmedicalcentre.com/symptoms.asp?sid=31&title=Hypercalcaemia#C3

http://erc.endocrinology-journals.org/content/12/3/549.full

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Categories
Ailmemts & Remedies Pediatric

Molar Pregnancy

Definition:
A molar pregnancy is one condition in a range of problems known as trophoblastic disease, where a pregnancy doesn’t grow as it should. It’s sometimes called a hydatiform mole.

There are two different types of molar pregnancy, which differ in how they form and how they need to be treated.

In a normal pregnancy, genetic material from the mother and father combines to form new life. In a molar pregnancy, this process goes wrong. In a complete molar pregnancy, the maternal chromosomes are lost, either at conception or while the egg was forming in the ovary, and only genetic material from the father develops in the cells. In a partial molar pregnancy, there is a set of maternal chromosomes but also two sets of chromosomes from the father (ie, double the normal paternal genetic material).

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The genotype is typically 46,XX (diploid) due to subsequent mitosis of the fertilizing sperm, but can also be 46,XY (diploid).  In contrast, a partial mole occurs when an egg is fertilized by two sperm or by one sperm which reduplicates itself yielding the genotypes of 69,XXY (triploid) or 92,XXXY (quadraploid).

Complete molar pregnancies develop as a mass of rapidly growing cells but without a foetus – it cannot therefore develop into a baby.
……
In a partial molar pregnancy, a foetus may start to develop but because of the imbalance in genetic material, it’s always abnormal and can’t survive beyond the first three months of pregnancy.

A molar pregnancy is often harmless, but if untreated can keep on growing and become invasive, spreading to the organs around it, or even further afield to the lungs, liver or brain. Very rarely, in two to three per cent of cases, it may become malignant. These cancerous types of trophoblastic disease are called choriocarcinoma and placental site trophoblast tumours.

Symptoms:
As the mole grows faster than a normal foetus would, the abdomen may become larger more quickly than would be expected for the dates of the pregnancy. The woman may experience abdominal pain, and also severe nausea and vomiting (hyperemesis).

Bleeding from the vagina is another common warning sign that things are not as they should be. Symptoms similar to pre-eclampsia – high blood pressure, protein in the urine, swelling of the feet and legs – may also occur in the first trimester or early in the second.

Most molar pregnancies are diagnosed at the first ultrasound scan, which shows a mass of cells without the presence of a foetus in a complete molar pregnancy or an abnormal non-viable foetus and placenta in a partial mole.

A woman with a hydatidiform mole often feels pregnant and has symptoms such as morning sickness, probably because the cells of the molar pregnancy produce the pregnancy hormone hCG (human chorionic gonadotrophin). This is also the hormone that is used in a pregnancy test, so she may have a positive result. Some women have no pregnancy symptoms (as with many normal pregnancies). — but most molar pregnancies cause specific signs and symptoms, including:

*Dark brown to bright red vaginal bleeding during the first trimester

*Severe nausea and vomiting

*Vaginal passage of grape-like cysts

*Rarely, pelvic pressure or pain

If you experience any signs or symptoms of a molar pregnancy, consult your health care provider. He or she may detect other signs of a molar pregnancy, such as:

*Rapid uterine growth — the uterus is too large for the stage of pregnancy

*High blood pressure

*Preeclampsia — a condition that causes high blood pressure and protein in the urine after 20 weeks of pregnancy

*Ovarian cysts

*Anemia

*Overactive thyroid (hyperthyroidism)

Causes:
A molar pregnancy is caused by an abnormally fertilized egg. Human cells normally contain 23 pairs of chromosomes. One chromosome in each pair comes from the father, the other from the mother. In a complete molar pregnancy, all of the fertilized egg’s chromosomes come from the father. Shortly after fertilization, the chromosomes from the mother’s egg are lost or inactivated and the father’s chromosomes are duplicated. The egg may have had an inactive nucleus or no nucleus.

In a partial or incomplete molar pregnancy, the mother’s chromosomes remain but the father provides two sets of chromosomes. As a result, the embryo has 69 chromosomes, instead of 46. This can happen when the father’s chromosomes are duplicated or if two sperm fertilize a single egg.

It remains unclear why a hydatidiform mole develops. However, there are a number of possible reasons, including defects in the egg, maternal nutritional deficiencies and uterine abnormalities. Women under 20 or over 40 are at higher risk.

Having a diet that’s low in protein, folic acid and carotene also increases the risk of a molar pregnancy. The number of times a women has been pregnant, however, doesn’t influence her risk.

Risk Factors:
Up to an estimated 1 in every 1,000 pregnancies is molar. Various factors are associated with molar pregnancy, including:

*Maternal age. A molar pregnancy is more likely for a woman older than age 35 or younger than age 20.

*Previous molar pregnancy. If you’ve had one molar pregnancy, you’re more likely to have another. The risk of a repeat molar pregnancy is 1 in 100.

*Some ethnic groups. Women of Southeast Asian descent appear to have a higher risk of molar pregnancy.

Diagnosis:
Molar pregnancies usually present with painless vaginal bleeding in the fourth to fifth month of pregnancy. The uterus may be larger than expected, or the ovaries may be enlarged. There may also be more vomiting than would be expected (hyperemesis). Sometimes there is an increase in blood pressure along with protein in the urine. Blood tests will show very high levels of human chorionic gonadotropin (hCG).

The diagnosis is strongly suggested by ultrasound (sonogram), but definitive diagnosis requires histopathological examination. On ultrasound, the mole resembles a bunch of grapes (“cluster of grapes” or “honeycombed uterus” or “snow-storm”). There is increased trophoblast proliferation and enlarging of the chorionic villi. Angiogenesis in the trophoblasts is impaired as well.

Sometimes symptoms of hyperthyroidism are seen, due to the extremely high levels of hCG, which can mimic the normal Thyroid-stimulating hormone (TSH).

Treatment :
Once it has been established that a woman is carrying a hydatidiform mole rather than a healthy foetus, suction evacuation is used to remove the pregnancy from the womb. This is curative in about four out of five molar pregnancies.

It’s then important to monitor the woman’s progress and repeatedly measure human chorionic gonadotropin (hCG) to be sure that everything settles back down to a normal, non-pregnancy level.

About 15 per cent of women who have had a complete molar pregnancy and 0.5 per cent of those with a partial molar pregnancy will require additional treatment, either because hCG levels hit a plateau or start to rise again, or because of persistent heavy vaginal bleeding.

Further treatment may involve the use of chemotherapy (usually methotrexate combined with folinic acid), especially if there’s any concern about invasive or malignant disease.

Complications:
After a molar pregnancy has been removed, molar tissue may remain and continue to grow. This is called persistent gestational trophoblastic disease (GTD). It occurs in about 10 percent of women after a molar pregnancy — usually after a complete mole rather than a partial mole. One sign of persistent GTD is an HCG level that remains high after the molar pregnancy has been removed. In some cases, an invasive mole penetrates deep into the middle layer of the uterine wall, which causes vaginal bleeding. Persistent GTD can nearly always be successfully treated, most often with chemotherapy. Another treatment option is removal of the uterus (hysterectomy).

Rarely, a cancerous form of GTD known as choriocarcinoma develops and spreads to other organs. Choriocarcinoma is usually successfully treated with multiple cancer drugs.

Prognosis:
More than 80% of hydatidiform moles are benign. The outcome after treatment is usually excellent. Close follow-up is essential. Highly effective means of contraception are recommended to avoid pregnancy for at least 6 to 12 months.

In 10 to 15% of cases, hydatidiform moles may develop into invasive moles. This condition is named persistent trophoblastic disease (PTD). The moles may intrude so far into the uterine wall that hemorrhage or other complications develop. It is for this reason that a post-operative full abdominal and chest x-ray will often be requested.

In 2 to 3% of cases, hydatidiform moles may develop into choriocarcinoma, which is a malignant, rapidly-growing, and metastatic (spreading) form of cancer. Despite these factors which normally indicate a poor prognosis, the rate of cure after treatment with chemotherapy is high.

Over 90% of women with malignant, non-spreading cancer are able to survive and retain their ability to conceive and bear children. In those with metastatic (spreading) cancer, remission remains at 75 to 85%, although their childbearing ability is usually lost.

Prevention:
Following successful treatment, most women can have children if they wish. However, it’s strongly recommended that a woman who has had a molar pregnancy doesn’t become pregnant again for 12 months. Although the likelihood is small, there’s a real risk of malignant disease developing and the increase in pregnancy hormones this would cause can’t be distinguished from those of a real pregnancy. Consequently, good contraception is required, as is regular monitoring by a hospital specialist.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Resources:
http://www.bbc.co.uk/health/physical_health/conditions/hydatidiformmole1.shtml
http://www.mayoclinic.com/health/molar-pregnancy/DS01155
http://en.wikipedia.org/wiki/Hydatidiform_mole

http://drugster.info/ail/pathography/375/

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Herbs & Plants

Cymopterus bulbosus

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Botanical Name :Cymopterus bulbosus
Family :Apiaceae
Genus : Cymopterus Raf.
Species : Cymopterus bulbosus A. Nelson
Kingdom : Plantae
Subkingdom :Tracheobionta
Superdivision : Spermatophyta
Division : Magnoliophyta
Class : Magnoliopsida
Subclass : Rosidae
Order : Apiales

Common Name :Biscuit Root

Habitat :South-western N. America – Wyoming to Texas and New Mexico. Dry hills and plains at elevations of 1200 – 2100 metres.

Description:
Cymopterus bulbosus is a perennial hurb. The flowers are hermaphrodite (have both male and female organs) and are pollinated by Insects.The plant is self-fertile.
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The plant prefers light (sandy), medium (loamy) and heavy (clay) soils and requires well-drained soil.The plant prefers acid, neutral and basic (alkaline) soils..It can grow in semi-shade (light woodland) or no shade.It requires dry or moist soil.

Propagation
Seed – we have no information on this species but suggest sowing the seed in a cold frame as soon as it is ripe if this is possible. Sow stored seed as early in the year as possible in a greenhouse. As soon as they are large enough to handle, prick the seedlings out into individual pots and grow them on in the greenhouse for at least their first winter. Plant them out into their permanent positions in late spring or early summer, after the last expected frosts. Division in spring or autumn might be possible

Edible Uses
Edible Parts: Condiment;  Leaves;  Root.

The root can be eaten raw, cooked or dried for later use. The dried leaves are used as a flavouring.  A celery flavouring. Leaves – cooked

Medicinal Uses:
The plant has been eaten as a stomach medicine.

Disclaimer:
The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider.

Sources:
http://www.pfaf.org/user/Plant.aspx?LatinName=Cymopterus%20bulbosus
http://www.swcoloradowildflowers.com/Pink%20Enlarged%20Photo%20Pages/cymopterus%20bulbosus%20and%20constancei.htm
http://plants.usda.gov/java/profile?symbol=CYBU
http://www.herbnet.com/Herb%20Uses_AB.htm

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Categories
Ailmemts & Remedies

Hydrocephalus

Definition:
Hydrocephalus, also known as “water on the brain,” is a medical condition in which there is an abnormal accumulation of cerebrospinal fluid (CSF) in the ventricles, or cavities, of the brain  and is an excessive amount of fluid that surrounds the brain and spinal cord called cerebrospinal fluid (or CSF).

This may cause increased intracranial pressure inside the skull and progressive enlargement of the head, convulsion, tunnel vision, and mental disability.The excess fluid can compress surrounding, fragile brain tissue, causing brain damage. Left untreated, hydrocephalus can be fatal. Hydrocephalus can also cause death.
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Hydrocephalus is sometimes present at birth, although it may develop later. About 1 out of 500 children is born with the disorder. The outlook if you have hydrocephalus depends on how quickly the condition is diagnosed and whether any underlying disorders are present.

The name derives from the Greek words  hudro means “water”, and kephalos means “head”.

Symptoms:
The clinical presentation of hydrocephalus varies with chronicity. Acute dilatation of the ventricular system is more likely to manifest with the nonspecific signs and symptoms of increased intracranial pressure. By contrast chronic dilatation (especially in the elderly population) may have a more insidious onset presenting, for instance, with the Hakim triad.

Symptoms of increased intracranial pressure may include headaches, vomiting, nausea, papilledema, sleepiness or coma. Elevated intracranial pressure may result in uncal and/or cerebellar tonsill herniation, with resulting life threatening brain stem compression. For details on other manifestations of increased intracranial pressure:

The triad (Hakim triad) of gait instability, urinary incontinence and dementia is a relatively typical manifestation of the distinct entity normal pressure hydrocephalus (NPH). Focal neurological deficits may also occur, such as abducens nerve palsy and vertical gaze palsy (Parinaud syndrome due to compression of the quadrigeminal plate, where the neural centers coordinating the conjugated vertical eye movement are located).

The symptoms depend on the cause of the blockage, the person’s age, and how much brain tissue has been damaged by the swelling.

In infants with hydrocephalus, CSF builds up in the central nervous system, causing the fontanelle (soft spot) to bulge and the head to be larger than expected. Early symptoms may also include:

*Eyes that appear to gaze downward (Sundowning)
*Irritability
*Seizures
*Separated sutures
*Sleepiness
*Vomiting

Symptoms that may occur in older children can include:

*Brief, shrill, high-pitched cry
*Changes in personality, memory, or the ability to reason or think
*Changes in facial appearance and eye spacing
*Crossed eyes or uncontrolled eye movements
*Difficulty feeding
*Excessive sleepiness
*Headache
*Irritability, poor temper control
*Loss of bladder control (urinary incontinence)
*Loss of coordination and trouble walking
*Muscle spasticity (spasm)
*Slow growth (child 0–5 years)
*Slow or restricted movement
*Vomiting

Hydrocephalus produces different combinations of these signs and symptoms, depending on its cause, which also varies by age. For example, a condition known as normal pressure hydrocephalus, which mainly affects older people, typically starts with difficulty walking. Urinary incontinence often develops, along with a type of dementia marked by slowness of thinking and information processing.

Causes:
In hydrocephalus, CSF builds up and puts pressure on the brain, squashing the delicate tissues and causing the chambers or ventricles within the brain to swell. Without treatment damage or destruction of the brain tissues may occur.

Our brain is the consistency of gelatin, and it floats in a bath of cerebrospinal fluid. This fluid also fills large open structures, called ventricles, which lie deep inside your brain. The fluid-filled ventricles help keep the brain buoyant and cushioned.

Cerebrospinal fluid flows through the ventricles by way of interconnecting channels. The fluid eventually flows into spaces around the brain, where it’s absorbed into your bloodstream.

Keeping the production, flow and absorption of cerebrospinal fluid in balance is important to maintaining normal pressure inside your skull. Hydrocephalus results when the flow of cerebrospinal fluid is disrupted — for example, when a channel between ventricles becomes narrowed — or when your body doesn’t properly absorb this fluid.

There are two types of hydrocephalus:
Non-communicating hydrocephalus – the flow of CSF through the brain is blocked.
Communicating hydrocephalus – either too much CSF is produced, or it isn’t reabsorbed back into the tissues as it should be, so volume increases.

There are many causes of hydrocephalus and some of them are:
•Bleeding in the brain (for example if a baby is born very preterm)
•Congenital malformations (structural abnormalities that are present from birth)
•After infections in the brain
•Brain tumours
•Abnormalities in the blood vessels in the brain

Defective absorption of cerebrospinal fluid causes normal pressure hydrocephalus, seen most often in older people. In normal pressure hydrocephalus, excess fluid enlarges the ventricles but does not increase pressure on the brain. Normal pressure hydrocephalus may be the result of injury or illness, but in many cases the cause is unknown.

Risk Factors:
Premature infants have an increased risk of severe bleeding within the ventricles of the brain (intraventricular hemorrhage), which can lead to hydrocephalus.

Certain problems during pregnancy may increase an infant’s risk of developing hydrocephalus, including:
*An infection within the uterus
*Problems in fetal development, such as incomplete closure of the spinal column

Congenital or developmental defects not apparent at birth also can increase older children’s risk of hydrocephalus.

Other factors that increase your risk of hydrocephalus include:
*Lesions or tumors of the brain or spinal cord
*Central nervous system infections
*Bleeding in the brain
*Severe head injury

Complications:
The severity of hydrocephalus depends on the age at which the condition develops and the course it follows. If the condition is well advanced at birth, major brain damage and physical disabilities are likely. In less severe cases, with proper treatment, it’s possible to have a nearly normal life span and intelligence.

Congenital:
The cranial bones fuse by the end of the third year of life. For head enlargement to occur, hydrocephalus must occur before then. The causes are usually genetic but can also be acquired and usually occur within the first few months of life, which include 1) intraventricular matrix hemorrhages in premature infants, 2) infections, 3) type II Arnold-Chiari malformation, 4) aqueduct atresia and stenosis, and 5) Dandy-Walker malformation.

In newborns and toddlers with hydrocephalus, the head circumference is enlarged rapidly and soon surpasses the 97th percentile. Since the skull bones have not yet firmly joined together, bulging, firm anterior and posterior fontanelles may be present even when the patient is in an upright position.

The infant exhibits fretfulness, poor feeding, and frequent vomiting. As the hydrocephalus progresses, torpor sets in, and the infant shows lack of interest in his surroundings. Later on, the upper eyelids become retracted and the eyes are turned downwards (due to hydrocephalic pressure on the mesencephalic tegmentum and paralysis of upward gaze). Movements become weak and the arms may become tremulous. Papilledema is absent but there may be reduction of vision. The head becomes so enlarged that the child may eventually be bedridden.

About 80-90% of fetuses or newborn infants with spina bifida—often associated with meningocele or myelomeningocele—develop hydrocephalus.

Acquired:
This condition is acquired as a consequence of CNS infections, meningitis, brain tumors, head trauma, intracranial hemorrhage (subarachnoid or intraparenchymal) and is usually extremely painful.

Effects:
Because hydrocephalus can injure the brain, thought and behavior may be adversely affected. Learning disabilities including short-term memory loss are common among those with hydrocephalus, who tend to score better on verbal IQ than on performance IQ, which is thought to reflect the distribution of nerve damage to the brain. However the severity of hydrocephalus can differ considerably between individuals and some are of average or above-average intelligence. Someone with hydrocephalus may have motion and visual problems, problems with coordination, or may be clumsy. They may reach puberty earlier than the average child (see precocious puberty). About one in four develops epilepsy.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Resources:
http://www.bbc.co.uk/health/physical_health/conditions/hydrocephalus2.shtml
http://www.mayoclinic.com/health/hydrocephalus/DS00393
http://en.wikipedia.org/wiki/Hydrocephalus

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